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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to determine the relative roles of O2 tension and content, CO2 tension, hydrogen ion concentration, arterial blood pressure, and cardiac output in the regulation of fetal cerebral blood flow (CBF), we used radioactively labeled microspheres to measure flow to 20 major brain regions in 24 chronically catheterized fetal lambs. We continually monitored fetal heart rate and blood pressure, and periodically measured arterial PO2, PCO2, pH, and hematocrit. In addition to CBF measurements during control periods, we measured CBF during: 1) hypoxia (O2 content less than 6 ml X dl-1; O2 tension less than 15 torr) induced by having the ewe breathe a gas mixture with low O2 concentration, 2) hypercapnia (PCO2 greater than 50 torr) induced by increasing the maternal inspired CO2, 3) acidosis and alkalosis (7.60 greater than pH greater than 6.60) induced by infusing lactic acid or bicarbonate into the fetus, and 4) hypotension (blood pressure less than 35 mm Hg) and hypertension (blood pressure greater than 55 mm Hg) induced by rapidly phlebotomizing or transfusing the fetus. We used multiple regression analysis and analysis of covariance to examine the dependence of total cerebral blood flow on arterial O2 tension and content, CO2 tension, pH, blood pressure, and cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional cerebral blood flow: studies in the fetal lamb during hypoxia, hypercapnia, acidosis, and hypotension. 644 Nov 42

Recurrent pulmonary embolism sometimes (3% of hospital autopsies) determines a progressive obstruction of the pulmonary vascular bed, which in turn causes pulmonary arterial hypertension and in time right ventricular hypertrophy and failure. The first stages of this process are characterized by slight pulmonary arterial hypertension at rest and by few and deceiving symptoms which make the diagnosis very difficult. Regarding anatomy, in most cases recurrent thromboembolism obstructs one of the main branches of the pulmonary artery. At the beginning pulmonary embolism usually manifests itself in a spontaneous and atypical manner: paroxysmal dyspnea, tachycardia, lateral chest pain, mild hemoptysis and recurrent fever. The clinical signs of peripheral thrombophlebitis are not very frequent. The chest roentgenogram supplies diagnostic information in 20% of cases, the electrocardiogram in 10%. Very important is the contribution of the analysis of arterial blood gases: hyperventilation, moderate hypoxia associated with shunting, hypocapnia with a widened difference between alveolar and arterial CO2. Pulmonary perfusion scintiphotography shows vast unperfused areas, different to the "plexogenic" appearance in primitive pulmonary arterial hypertension, in about 50% of cases. Pulmonary angiography discloses the exact site and extension of the obstruction in 80-90% of cases. On catheterization pulmonary arterial hypertension results to be inconstant and may appear only during stress. Regarding the evolution of pulmonary embolism, the forms associated with pulmonary arterial hypertension may last several years, although recurrent embolism may shorten its course. When the stage of right ventricular hypertrophy is reached, the evolution is generally rapid (from 1 to 4 years).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pulmonary thromboembolism. 653 60

Spinal cord tissue oxygen was measured by polarography at the dorsum of the spinal cord for 24 hours after acute spinal cord injury, and the effects of hypertension, hypercarbia, and hyperoxia were examined. Acute spinal cord injury was produced in mongrel dogs by constriction of the midthoracic cord with an epidural tourniquet inflated to 400 mm Hg, which was maintained for 5 minutes. At the injury site spinal cord tissue oxygen was slightly increased immediately after injury but was depressed significantly at 1 hour and remained unchanged thereafter. Hypertension induced by the intravenous infusion of norepinephrine elevated the tissue oxygen only slightly after 3 hours. Hypercarbia and hyperoxia produced by ventilation with a 95% O2:5% CO2 mixture did not elevate the depressed spinal cord oxygen content. When hypertension, hypercarbia, and hyperoxia were combined, the spinal cord oxygen value was elevated to the normal level even at 3 hours after injury, when the cord oxygen was at its lowest, and it increased steadily thereafter.
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PMID:Effects of hypertension and hypercarbia on spinal cord tissue oxygen in acute experimental spinal cord injury. 677 23

Combined hypertension and hypercarbia, which was found to improve post-traumatic spinal cord hypoxia and presumably ischemia in our previous study, was used in dogs subjected to experimental spinal cord injury to determine its therapeutic effects against acute spinal cord trauma. Intermittent hypertension and hypercarbia therapy, in which 15 minutes of hypertension and 95% O2:5% CO2 gas ventilation were alternated with 10 minutes of air ventilation, was given for 3 hours beginning 3 hours after injury. The treated dogs and untreated control dogs were checked neurologically and electrophysiologically at weekly intervals for up to 8 weeks. The treated dogs showed higher grades of neurological function within 1 week, but the results were statistically insignificant. Both groups demonstrated steady neurological improvement for the next 2 weeks and remained paraparetic thereafter with no group difference. The size of the intramedullary lesion was identical in both groups. Recovery of the somatosensory evoked potentials coincided well with neurological improvement, with again no difference between the two groups.
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PMID:Therapeutic trial of combined hypertension and hypercarbia on experimental acute spinal cord injury. 677 24

The effect of captopril treatment (100 mg/kg by mouth daily for up to 6 months) on pressor responses to norepinephrine (NE) and angiotensin II (AII) was examined in spontaneously hypertensive rats (SHR). Also, helical strips of rat aorta were removed from rats that had been similarly dosed. The aortic strips were suspended for isometric recording in modified Krebs' solution kept at 37 degrees C and bubbled with 95% O2-5% CO2. Pressor responses of both NE and AII in vivo were inhibited by captopril in SHR treated for all treatment periods. Responses to NE were more significantly and consistently inhibited than those for AII. Aortic strips from SHR previously dosed with captopril showed equivalent or greater contractile responses to potassium chloride (KCl) and NE, when compared with strips from untreated age-matched controls. In aortic strips from untreated Sprague-Dawley rats incubated with captopril, 30 micron g/ml for 1 hour ( a concentration 6000 times higher than that needed to inhibit angiotensin-covering enzyme by 50% in vitro), captopril had no effect on nitroglycerin-induced relaxation or NE-induced contractions, whereas ethacrynic acid (25 micron g/ml) reduced both the NE contractile response as well as the nitroglycerin-induced relaxation. These results suggest that captopril has no direct effect on the ability of isolated vascular smooth muscle to contract or relax despite causing a significant inhibition of pressor responses in vivo. It is suggested that this effect is related to an interaction of captopril with blood-borne elements necessary for the full expression of vasoconstriction, but unrelated to angiotensin-converting enzyme inhibition.
Hypertension
PMID:Effects of captopril on vascular reactivity of SHR in vivo and in vitro. 679 15

The role of CO2 in hyperbaric oxygen toxicity was investigated by administering acetazolamide (Diamox), Tris buffer [tris(hydroxymethyl)aminomethane], and sodium bicarbonate by i.p. injection, and by exposure of other groups of animals to an atmosphere of 5% CO2 and 95% O2. All animals were placed in a pressure chamber and maintained at 50 psig in 100% O2 until death. The Tris buffer and the sodium bicarbonate buffer significantly extended time to onset of convulsions and to time of death. Acetazolamide and also 5% CO2 shortened time to onset of convulsions and significantly shortened survival time. These results suggest that increased tissue levels of CO2 play an important role in hyperbaric oxygen toxicity. The cause of death in our animals exposed to hyperbaric oxygen was pulmonary edema secondary to a systemic hypertension.
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PMID:Acetazolamide and CO2 in hyperbaric oxygen toxicity. 680 59

Systems analysis of the systemic arterial (SAPW), cerebrospinal fluid (CSFPW), and sagittal sinus (SSPW) pulse waves was carried out in 13 dogs during hypercapnia (5% CO2), intracranial normotension (inhalation of 100% O2), and intracranial hypertension (inhalation of 100% O2 plus an intraventricular infusion). Power amplitude and phase spectra were determined for each wave, and the power amplitude and phase transfer functions calculated between the cerebrospinal fluid (CSF) pressure and systemic arterial pressures, and between the sagittal sinus pressure and CSF pressure. The study indicates that the CSFPW and SSPW were virtually identical when impedance between the cerebral veins and sagittal sinus was minimal, which argues that the CSF pulse was derived from the cerebral venous bed. During inhalation of 100% O2, transmission of the SAPW across the precapillary resistance vessels into the cerebral venous pulse (as represented by the CSFPW) was nonlinear, while transmission across the lateral lacunae into the sagittal sinus was linear. During intracranial hypertension, wave transmission across the precapillary resistance vessels was linear, and across the lateral lacunae was nonlinear. During hypercapnia, wave transmission across the precapillary resistance vessels and the lateral lacunae was linear. When the wave transmission was nonlinear, there was also suppression in transmission of the lower harmonics, particularly the fundamental frequency, and a more positive phase transfer function, suggesting an inertial effect or decrease in acceleration of the pulse. Conversion from a nonlinear to linear transmission across the precapillary resistance vessels is evidence of loss of vasomotor tone, and is accompanied by rounding of the CSFPW. A vascular model which encompasses the above data and is based on flow in collapsible tubes and changes in vasomotor tone is posited to explain control of pulsatile flow and pulse waveform changes in the cerebrovascular bed. The model helps to clarify the strong interrelationship between intracranial pressure, cerebral blood flow, and cerebral autoregulation.
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PMID:Cerebrospinal fluid pulse waveform as an indicator of cerebral autoregulation. 706 79

In 27 pentobarbital-anesthetized cats cerebral blood flow and regulation of cerebral blood flow was measured one to 3 weeks following stereotactical xenotransplantation of a rat glioma clone into the internal capsula. Tumor growth was accompanied by severe vasogenic peritumoral edema in the white matter of the tumor-bearing hemisphere. White matter water content in the vicinity of the tumor increased from 69.1 +/- 0.9 to 0.5 +/- 0.7 ml/100 g wet weight (means +/- SE) which corresponds to an increase in tissue volume of about 60%. Intracranial pressure after 3 weeks was 12 +/- 2.6 mm Hg. Blood flow in the peritumoral white matter decreased from 32.2 +/- 5.6 to 18.6 +/- 1.9 ml/100/g/min but it did not change in the peritumoral grey matter or the opposite hemisphere. The decrease in blood flow was due to the volume expansion of the swollen edematous tissue and not to a compression of the microcirculation because neither flow nor vascular resistance changed when referred to dry rather than to wet weight of the edematous tissue. Flow regulation in the peritumoral edematous white matter was disturbed. CO2 reactivity of blood flow was 5.4% mm Hg change in aPCO2 (non-edematous contralateral white matter 6.4%/mm Hg), and the autoregulatory capacity between 40 and 170 mm Hg was 0.7%/mm Hg (non-edematous white matter 1.0% mm Hg). It is concluded that in the absence of significant intracranial hypertension, even severe degrees of vasogenic peritumoral edema do not interfere with blood flow and flow regulation. This is in contrast to the cytotoxic type of edema, and indicates that microcirculatory compression by edema, when present, is the consequence of pericapillary glial hydrops and not of an accumulation of extravasated edema fluid.
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PMID:Blood flow and regulation of blood flow in experimental peritumoral edema. 723 66

The sitting position in neurosurgery gives always three problems for the anaesthesist: --maintain the cerebral perfusion pressure, --not to aggravate intracranial hypertension, --detect gaseous embolism. The clinical signs of air embolism often look like the awakening of the patient. That is why it is necessary to use specific methods to detect them: Doppler, Swan-Ganz catheter, and/or continuous CO2 recording of expired air by capnograph. Among the various methods to prevent air embolism we have used controlled respiration with a positive and expiratory pressure (P.E.E.P.). In our series (45 operations) gas embolism occurred in 13% of the patients operated upon without positive and expiratory pressure, and 0% with P.E.E.P.
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PMID:[The technique of anesthesia for the prevention and treatment of gaseous embolism in the neurosurgical sitting position (author's transl)]. 745 51

This study tested the hypothesis that breathing at the upper end of the normal range of end tidal CO2 decreases renal sodium excretion. Normotensive human subjects learned to self-regulate end tidal CO2 using a respiratory gas monitor and feedback procedure. Urine flow rates were increased by a standardized water drinking regimen. Urinary volume and sodium and potassium excretion were decreased during 30 minutes of inhibited (i.e. high normal end tidal CO2) breathing, compared with levels preceding and after task performance. Blood pressure, but not heart rate, increased during task performance. Plasma volume increase under these conditions is indicated by the observation that urinary excretion of an endogenous digoxin-like factor was increased. The physiological mechanism by which inhibited breathing elicits renal sodium retention remains to be determined. This breathing pattern could mediate the role of behavioral stress in some forms of hypertension.
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PMID:Inhibited breathing decreases renal sodium excretion. 748 May 67


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